Ask about this productRelated genes to: IP6K1 antibody
- Gene:
- IP6K1 NIH gene
- Name:
- inositol hexakisphosphate kinase 1
- Previous symbol:
- IHPK1
- Synonyms:
- KIAA0263
- Chromosome:
- 3p21.31
- Locus Type:
- gene with protein product
- Date approved:
- 2002-03-11
- Date modifiied:
- 2009-01-05
Related products to: IP6K1 antibody
Related articles to: IP6K1 antibody
- Necrotizing enterocolitis (NEC) is a life-threatening intestinal inflammatory disease in preterm infants. Inositol hexakisphosphate kinase 1 (IP6K1) regulates platelet polyphosphate (polyP) homeostasis, yet its roles in NEC remain unclear. - Source: PubMed
Publication date: 2026/06/20
Gao KaiZhu MuyangLiu QianyangMa YueXu HongmeiGuo Chunbao - High protein diets (HPD), rich in branched-chain amino acids (BCAAs), are proposed to enhance glycemic control. The metabolic implications of elevated BCAAs in insulin resistance (IR) are unclear, but overactivation of ribosomal protein S6 kinase B1 (S6K1)-related signaling pathway may contribute to IR. - Source: PubMed
Publication date: 2026/01/28
Ancu OanaHauge-Evans Astrid CDraicchio FulviaNeculescu Diana-ElenaRogers RalphBurd Nicholas APfeiffer Andreas F HWeickert Martin OHurren Nicholas MMackenzie Richard W A - Inositol hexakisphosphate kinases (IP6Ks) catalyze the synthesis of the inositol pyrophosphate 5-InsP, and regulate diverse physiological processes. mice display reduced body weight despite normal food intake, elevated fecal protein, and reduced skeletal muscle mass compared with mice, suggesting that IP6K1 may support protein digestion. IP6K1 is expressed throughout the mouse gastrointestinal tract, and is especially enriched in the cytoplasm of chief cells in the stomach, which are responsible for the storage and secretion of digestive enzymes. Pepsinogen C (PGC) containing granules were sparse, and gastric lipase F granules were completely absent in the gastric glands of mice, despite normal expression levels of these enzymes, implicating IP6K1 in digestive enzyme granule biogenesis. The level of the active protease pepsin C was decreased in the gastric lumen of mice compared with mice. CRISPR/Cas9-mediated deletion of IP6K1 in the gastric adenocarcinoma cell line AGS recapitulated the phenotype of reduced PGC granules seen in gastric chief cells of mice. PGC granule formation was restored in AGS cells by the reintroduction of catalytically active or inactive IP6K1, indicating that IP6K1 supports the formation of secretory granules independent of its enzymatic activity. The proteoglycan SDC4, identified as an interactor of IP6K1, was seen to colocalize and comigrate with PGC granules in but not in AGS cells. Our findings identify IP6K1 as a novel regulator of secretory granule biogenesis in gastric chief cells, to influence protein digestion in the mammalian stomach. Through detailed phenotypic analysis of mice and mechanistic studies, we identify IP6K1 as a key regulator of digestive enzyme granule biogenesis and secretion in gastric glands. IP6K1 is shown to act via its specific interactor, the proteoglycan syndecan-4 (SDC4), to mediate pepsinogen C granule biogenesis. By extending IP6K1's functional landscape into gastrointestinal biology, our study opens new avenues for understanding its impact on digestion and metabolic health. - Source: PubMed
Publication date: 2026/04/29
Sen JayrajPore PranjaliBhandari Rashna - Inorganic polyphosphate (polyP) is a linear polymer of phosphate residues linked by phosphoanhydride bonds. PolyP remains poorly understood in mammals due to its low abundance and lack of information on its metabolism. We developed a DAPI fluorescence-based assay to quantify the low levels of polyP present in mammalian cell lines and tissues, detecting an enrichment of polyP in the mitochondria compared with the nucleus and post-mitochondrial fraction. Mitochondrial polyP synthesis was found to depend on active FoF1 ATP synthase and an intact proton gradient across the inner mitochondrial membrane. Additionally, orthophosphate (Pi) is essential for mitochondrial polyP production, and ATP enhances Pi-driven polyP synthesis in isolated mitochondria. We discovered that the inositol pyrophosphate 5-InsP, synthesized by IP6K1, regulates mitochondrial polyP levels. Mice and cells deficient in IP6K1 showed a significant reduction in mitochondrial polyP synthesis compared with wild type controls. Cells lacking IP6K1 also showed impaired mitochondrial respiration. The expression of active IP6K1, but not its catalytically inactive form, restored mitochondrial polyP synthesis in IP6K1 deficient cells, but mitochondrial respiration was rescued by expression of either active or inactive IP6K1. These data show that IP6K1 regulates mitochondrial function and polyP production both through the synthesis of 5-InsP and via a catalytic activity-independent mechanism. Our findings uncover a link between 5-InsP, an energy sensor, and polyP, an energy store, in the regulation of mammalian mitochondrial homeostasis. - Source: PubMed
Publication date: 2026/03/31
Ladke Jayashree SKhan AzmiSingh AnshitJessen Henning JKolthur-Seetharam UllasJaiswal ManishBhandari Rashna - Age-related muscle mass is driven by a reduction in insulin sensitivity partly mediated by reduced amino acid and anabolic signalling kinetics. Insulin activates Akt-mTORC1 signalling in skeletal muscle, with inositol hexakisphosphate kinase 1 (IP6K1) shown to inhibit this signalling pathway in pre-diabetic humans. We aimed to compare muscle and plasma IP6K1 in young vs older adults and the possible role of IP6K1 in the anabolic response to protein and protein plus resistance exercise (RE). Nine young (24.9 ± 0.4 years) and nine older (66.2 ± 0.5 years), moderately active adults received primed continuous infusions of L-[ring-H]phenylalanine in basal and postprandial state. Blood and muscle biopsy samples were collected prior to and following ingestion of 25 g whey protein with or without knee extension exercise to examine skeletal muscle protein signalling and whole-body phenylalanine kinetics. Young adults had greater plasma IP6K1 at all time points. Older adults had reduced muscle IP6K1 at 120 min post-exercise. Muscle IP6K1 decreased 240 min postprandially in young adults compared with basal and there was no effect of exercise in either group. Older adults presented with reduced plasma and muscle IP6K1 in both postprandially and post-RE states, as well as reduced phenylalanine rate of disappearance for the same comparisons. IP6K1 may be involved in the reduction in amino acid metabolism and the insulin-mediated response to protein and RE. - Source: PubMed
Publication date: 2026/02/18
Barclay Richie DMotei Diana EAncu OanaTyler Christopher JTillin Neale ABehrends VolkerBurd Nicholas AHurren Nicholas MMackenzie Richard W A